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Alterations in Sodium
• Sodium
○ Helps conduct neural impulses, helps reg K+, found in all body
fluids, neurological responses.
○ nml: 135 to 145 mEq/L (each lab has own normals)
○ Hyponatremia below 135
Causes
Renal disease
Diuretics
GI losses
Skin Losses
Wound drainage
○ Hypernatremia above 145
Causes
Decreased water intake
Watery diarrhea
Fever
Hyperventilation
Burns
Increased sodium dietary intake
• What happens to people?
○ hyponatremia
• behavioral changes
lethargy
confusion
• depressed reflexes
• seizures
• coma
○ hypernatremia
• thirst
• fever
• dry mucous membranes
• restlessness
• Alterations in Potassium
○ Potassium, even small changes are poorly tolerated.
• Functions: maintains action potentials of muscles, assists in
controlling the cardiac rates/rhythms, conducts nerve
impulses.
○ nml: 3.5 to 5 mEq/L
○ Mechanisms of regulation
renal regulation
Kidneys maintain balance by excreting or reabsorbing
in glomerulus (mostly).
Extra- and intra cellular shifts
Temporary shift into RBC (hemoglobin), liver muscles,
bone
○ Hypokalemia
Low intake in diet, excessive loss of K+ usually in gut
(suctioning), nausea/vomiting, sweating profusely, diabetes
encephalitis.
○ Hyperkalemia
Excessive intake of potassium, usually body tolerates well
unless a lot given quickly, renal failure, potassium sparing
diuretics.
• What happens to the person
○ Hypokalemia
Mild losses asymptomatic
Well tolerated
Acute Losses cause
Skeletal Muscle Weakness
Loss of smooth muscle tone
Cardiac dysrhythmias
Lethargy/Fatigue
Inability to concentrate
○ Hyperkalemia
Slow onset usually well tolderated
Mild
Restless ness
Intesting cramping
Diarrhea
Severe: (see slide)
• Alterations in Calcium and Phosphorus and Magnesium
○ Vitamin D regulation
Calcitriol - form of vit D makes Ca and Phosphorus available
for bone mineralization.
Helps absorb Ca in intestine.
Activates parathyroid hormone.
○ Parathyroid hormone regulation
Helps increase blood calcium levels by transporting Ca out
of bones.
Aid reabsorption in kidneys
Raise serum Ca levels and lowers Phosphorus levels b/c
they have an inverse relationship with one another.
• Alterations in Calcium
○ Muscle contractions, clotting abil, neurological conduction,
rigidity to teeth/bones.
○ Normal level 8.5-10.5 mg/dl
○ Hypocalcemia
Causes
Hypoparathyroidism
Hypomagnesemia
Alkalosis
Multiple blood transfusions
Malabsorptive states
Renal disease
○ Hypercalcemia
Causes
Hyperparathyroidism
Hypophosphatemia
Hyperthyroidism
Vitamin D intoxication
Steroid therapy
Immobility
Lithium therapy
• Alterations in Calcium
○ hypocalcemia
Paresthesias (muscle pain)
skeletal muscle cramps
abdominal spasms and cramps
hyperactive reflexes
Hypotension
bone pain, deformities, factures
○ hypercalcemia
Polyuria (a lot of peeing), polydipsia (very thirsty)
anorexia, n/v, constipation
Ataxia (uncoordinated muscle movements)
osteoporosis
lethargy
stupor, coma
HTN - may be due to inabil of muscle cells to relax fully.
• Alterations in Phosphorus (Phosphate)
○ Inverse relationship with Ca, essential for muscular function,
important for RBC function, cellular metabolism, role in
formation of teeth/bones.
○ Normal level: 2.5 to 4.5 mg/dl
○ Hypophosphatemia
From decreased absorption of Vit D, intestinal loss, less skin
absorption, diabetic ketoacidosis, alcoholic, poor dietary
intake.
○ Hyperphosphatemia
From renal insufficiency, low blood calcium, chemotherapy,
parathyroid gland is understimilated, prolonged Vit D
exposure, antacids, salicylates, excessive intake of phos
supplements, massive transfusions of blood.
• Alterations in Phosphorus Manifestations
• Hypophosphatemia
○ Intention tremor
○ Ataxia, Paresthesias
○ Seizures
○ muscle weakness
○ bone pain
○ Osteomalacia (softening of bone)
○ bleeding disorders
○ impaired WBC fxn
• Hyperphosphatemia
○ paresthesias
○ Tetany (rigidity to muscles)
○ hypotension
○ cardiac arrhythmias
• Alteration in Magnesium
○ Usually a function of dietary intake, role in enzymatic process in
body, helps power Na/K pump (convert ATP to ADP), transmits
electrical impulses across nervous system and MSK, necessary
to release parathyroid hormone.
○ Normal level: 1.8 to 3.0 mg/dl
○ Hypomagnesia
Chronic alcoholism (most common)
Decreased dietary intake
Decreased absorption d/t GI pathology
Increased GI losses
Increased Renal excretion
Burns
○ Hypermagnesia
Untreated diabetic ketoacidosis
Adrenal insufficiency
Mg++ treatment in preeclampsia (pregnancy induced HTN)
Lithium ingestion
Volume Depletion
• Alteration in Magnesium Manifestations
• hypomagnesia
○ personality change
○ nystagmus
○ tetany
○ tachycardia
○ hypertension
○ cardiac arrhythmias
○ + Babinski, Chvostek, and Trousseau signs
• hypermagnesia
○ Lethargy
○ Hyporeflexia
○ Confusion
○ Coma
○ Hypotension
○ Cardiac arrhythmias
○ cardiac arrest
• Acid Base Disturbances
• Acid-Base Balance
○ Must be regulated in a narrow range to function normally
○ Lungs, kidneys, and bone regulate the balance
○ Hydrogen ions maintain membrane integrity and speed
enzymatic reactions
○ Bicarbonate is maintained as well.
○ pH represents a power of hydrogen
○ pH < 7.4 is acidic, > 7.4 alkaline
• Buffers
○ Absorb excess H+ and OH-
○ Prevent significant change in pH
○ Exist as acid base pairs
○ Carbonic Acid Buffering (bicarb) [main system]
Lungs and kidneys
Changing rate of ventilation (blow off extra CO2 or retain)
Retain bicarb or excrete extra in pee.
○ Protein Buffering (hemoglobin)
CO2 loaded onto hemoglobin
○ Renal Buffering (phosphate)
Secreting H ions in urine and reabsorbing bicarb in renal
tubules.
• Acid Base Disorders
○ Metabolic versus Respiratory
Metabolic - produce and alteration in bicarb (hydrogen and
CO2 associates and disassociates to be moves through
system),
Respiration - alteration in partial pressure of CO2, increase
or decrease in ventilation
○ Acidotic versus Alkalotic
pH level
• Metabolic Acidosis
○ Decrease HCO3- with decrease pH
○ Causes
Diabetic Ketoacidosis, kidney failure, aggressive suctioning
of the GI tract
○ Compensation in increased resp. rate (blow off CO2) Kussmaul
type respiration.
○ Treatment
Treat underlying cause, replace fluid/electrolyte volume.
Supplemental sodium bicarb if severe (IV)
• Metabolic Alkalosis
○ Increased pH due to primary excess of HCO3-
○ Causes
Increase in intake of alkalotic solution (IV, oral [antacids]),
vomiting, binge purge.
○ Compensation
Decrease respiratory rate and depth
Kidneys bring down pH by excreting more HCO3 in urine
(basic urine).
○ Treatment
With fluid replacements.
• Acid Base Imbalances
○ Metabolic Acidosis
Early:
HA (head ache)
lethargy
Severe:
Coma
Death
Compensatory Mechanism
Kussmaul respirations
○ Metabolic alkalosis
Weakness
Muscle cramps
Hyperactive reflexes
Tetany
Shallow, slow respirations
Confusion
Convulsions
Atrial tachycardia
• Respiratory Acidosis
○ impaired alveolar ventilation and increase in PCO2 along with
decrease in pH
○ Causes
Respiratory disorder (pneumonia, pulmonary edema,
respiratory distress syndrome, damage muscles of chest
wall, extremely obese (limited movement of chest wall),
○ Compensation
Conserve and generate bicarb in body
Kidneys excrete H+.
○ Treatment
Improve ventilation status (mechanical ventilator).
• Respiratory Alkalosis
○ decrease in PCO2 producing an elevated pH and increase in
HCO3-
○ Causes
Anxiety attack (psychogenic hypoventilation), hypoxia
caused by some form of lung disease, problem with
stimilation to ventilate, problem with respiratory center of
brain, mechanical vent w/ incorrect vent settings.
○ Compensation
Eliminated bicarb in kidneys, conserve H+
○ Treatment
Underlying cause, supplemental oxygenation, change
ventilation settings, anxiety - reassurance.
• More Acid-Base Imbalances
○ Respiratory Acidosis
First:
Breathlessness
Restlessness
Apprehension
Then:
Lethargy
Disorientation
Muscle twitching
Tremors
Convulsions
Coma
○ Respiratory Alkalosis
Dizziness
Confusion
Tingling of extremities
Convulsions
Coma
Deep rapid respirations are the primary symptom
• Serum lab values (will be posted on Moodle)